We examined the effect of dilazep dihydrochloride (dilazep) on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats (SHRs). Ataxia and loss of the righting reflex were noted in some SHR after 4 hr occlusion of the bilateral common carotid arteries; and 11 of 15 animals died within 72 hr after reperfusion. One hour after reperfusion, the cerebral water content increased significantly. The chemiluminescence value in the brain homogenate increased slightly during occlusion; and following reperfusion, there was a transient but marked further increase, indicating the acceleration of lipid peroxidation that resulted from free radical reactions. The i.v. infusion of dilazep (0.3-3 mg/kg/hr for 4 hr) during occlusion dose-dependently reduced the appearances of neurological symptoms and mortality during occlusion and after reperfusion. The increase in cerebral water content and chemiluminescence value were clearly prevented by dilazep (3 mg/kg/hr). It is concluded that dilazep possesses the ability to prevent the appearances of neurological symptoms and brain edema induced by ischemia and reperfusion. The suppression of lipid peroxidation may be involved in the mechanism of the preventive effect of dilazep on cerebral injury.